Aging enhances vascular dysfunction induced by the Alzheimer's peptide beta-amyloid
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Updated: Aug 24, 2026

In Vitro Assays to Assess Blood-brain Barrier Mesh-like Vessel Formation and Disruption
Published on: June 20, 2017
Joel M Price1, Alison Hellermann, Gary Hellermann
1Department of Physiology and Biophysics, University of South Florida, College of Medicine, Tampa, Florida 33612, USA. jprice@hsc.usf.edu
Abstract:
Aging is a major risk factor for Alzheimer's disease and the evidence suggests a role for cerebrovascular pathology in cognitive dysfunction. The hypothesis in this study is that aging is a significant risk factor in the effect of the Alzheimer peptide beta-amyloid on endothelium-dependent function of cerebral and peripheral vessels. The diameter response to acetylcholine, an endothelium-dependent vasodilator, was recorded in pressurized segments of rat posterior cerebral vessels from mature (3 months) and aged (20 months) rats. The threshold concentration of beta-amyloid for a significant decrease in the response to acetylcholine was lower in vessels from aged rats (10(-9) M) than in vessels from mature rats (10(-8) M). The threshold concentration of beta-amyloid for a significant decrease in the sensitivity to acetylcholine was lower for ring segments of aorta from aged rats (10(-10) M) than for aorta from mature rats (10(-8) M). Structural changes of the endothelium were first observed in electron micrographs of aorta from aged rats when the concentration of beta-amyloid was 10(-8) M, whereas structural changes in aorta from mature rats did not occur until the concentration of beta-amyloid was increased to 10(-7) M. The results suggest that aging increases the susceptibility of cerebral and peripheral blood vessels to beta-amyloid related dysfunction and that functional change precedes structural change.
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